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Step 1 - Elise > UWorld Gastrointestinal Physiology > Flashcards

UWorld Gastrointestinal Physiology Flashcards

1
Q

What is the postprandial alkaline tide?

A

Increase in plasma bicarb and decrease in plasma Cl- secondary to surge of acid in the lumen.

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2
Q

What helps most to downregulate gastric acid secretion after a meal?

A

intestinal influences - ileum and colon release peptide YY to bind to ECL to decrease histamine, as well as SOMATOSTATIN and PGs (both Gi –> decrease cAMP)

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3
Q

Location of ileum with a large role in recycling bile acids. What disease affects this area, resulting in increased possibility of gallstones?

A

terminal ileum - Crohn Disease

Bile acids are produced in the liver, excreted with bile, reach terminal ileum to absorb cholesterol and return to liver. When terminal ileum is inflamed, bile acids cannot be reabsorbed. So less bile acid is available for secretion from liver and cholesterol can precipitate in bile and cause gallstones.

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4
Q

what class of drug inhibits the RLS of bile acid synthesis (cholesterol 7-alpha-hydroxylase). SE?

A

Fibrates.

SE - may develop cholesterol gallstones dt supersaturation of bile with cholesterol.

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5
Q

What class of drugs inhibits RLS of cholesterol synthesis (HMG CoA-Reductase), reducing risk of gallstone formation?

A

statins

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6
Q

Deficiency in what enzyme leads to both protein and fat malabsorption? A newborn would present with FTT, diarrhea, and edema.

What is the function of this enzyme?

A

Enteropeptidase from jejunal brush border, which cleaves inactive trypsinogen to form active trypsin. Trypsin then goes on the activate all other pancreatic enzymes.

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7
Q

Bile acid conjugation with glycine and taurine form _____. Why is this good?

A

Form bile salts, increasing their solubility and ability to digest lipids.

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8
Q

What do chief cells secrete?

A

Pepsinogen.

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9
Q

What do parietal cells secrete?

Name the three receptors/receptor types.

A

H+ and IF.
Receptors:
1. M3 receptor (Gq) , stimulated by ACh from vagus nerve.
2. CCK-B receptor (Gq) , stimulated by gastrin from G cells.
3. H2 receptor (Gs), stimulated by histamine from ECL cells.

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10
Q

Location of dietary lipid digestion.

Location of dietary lipid absorption.

A

Digestion in duodenum my pancreatic enzymes. Bile salts (and phosphatydlcholine) emulsify breakdown products, forming water soluble micelles.
Absorption in the jejunum.

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11
Q

Gallbladder secretes ___. Secretion is stimulated by ___.

What if the enzyme is not present?

A

Secretes bile from liver. Stimulated to release bile via contraction dt CCK stimulation. CCK is released from I cells in duodenum and jejunum when fat-protein-rich chyme enters duodenum.

Lack of CCK can lead to biliary stasis –> gallstone formation.

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12
Q

Crohn Disease is associated with ___ kidney stone. Why?

A

OXALATE kidney stones because impaired bile acid absorption in the terminal ileum leads to loss of bile acids in feces with subsequent fat malabsorption. Lipids bind to Ca-ions and make a soap complex. Free oxalate (normally bound by Ca to form unabsorbable complex) is absorbed and forms urinary calculi (enteric oxaluria).

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13
Q

What stones are caused by Proteus and Kelb?

A

struvite stones, made of Magnesium Ammonium Phosphate (struvite) and Calcium Carbonate-Apatite. Form bc of alkalization of urine.

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14
Q

Function of pancreatic amylase.

A

To degrade polysaccharides (unabsorbable) into monosaccharides.

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15
Q

What does the pancreas release?

A 
Pancreatic amylases (protein digestion) - secretes trypsinogen activates the proteases.
Pancreatic lipases (fat digestion).
High levels of bicarb.
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16
Q 
What is secreted by:
S cells in gastric antrum and duodenum
D cells of pancreatic islets and gut mucosa
I cells of small intestine
S cells of small intestine
K cells of small intestine
M cells of small intestine
A

Gastrin –> incr gastric acid secretion
Somatostatin - decrease most GI hormone secretion
CCK - increase pacnreatic enzyme and bicarb secretion
Secretin - increase pancreatic bicarb secretion, decrease gastric acid secretion
GIP - increase insulin release, decrease gastric acid secretion
Motilin - increase GI motility

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17
Q

Elevated serum Amino-transferalse levels due to massive hepatocellular injury, prolonged PTT dueto failure of hepatic synthetic function, leukocytosis, eosinophilia. Widespread liver inflammation –> fulminant hepatitis.

Possible cause.

A

Inhlaed anesthetics (i.e. halothane) leading to highly lethal fulminant hep, indistinguishable form acute viral hepatitis.

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18
Q

Lactase deficiency causes what changes to the following:

  • breath hydrogen content
  • stool osmotic gap
  • stool pH
A
  • increased breath hydrogen content
  • increased osmotic gap of stool bc of unmeasured/undigested lactose
  • decreased stool pH due to undigested lactose
19
Q

Sx: fatigue, itching, HM
Labs: serum ALK-phos elevated, antimitochondrial ab present
Biopsy: patchy lymphocytic inflammation with destruction of small and mid-sized intrahepatic bile ducts and necrosis and microbodular regeneration of periportal tissues. Also common are granulomas and bile staining of hepatocytes.

Two DDx?

A

Primary biliary cirrhosis or graft-v-host disease

20
Q

liver failure with centrilobular necrosis that can extend to includ ethe entire lobe

A

serious acetaminophen overdose

21
Q

hepatocellular swelling and necrosis, Mallory bodies, neutrophilic infiltration, and fibrosis

A

alcoholic hepatitis

22
Q

HM with tense capsule and reddish purple parenchyma. Severe centrilobular congestion and necrosis.

A

Budd chiari (hepatic vein occlusion)

23
Q

deposition of hemosiderin in liver. Non inflammatory necrosis with fibrosis

A

hemochromatosis

24
Q

KIT receptor tyrosine kinase mutation.
Sx: flushing, syncope, hypotension, pruritis, urticaria, abdominal cramping (hypersecretion of gastric acid), diarrhea.

What is it?

A

Systemic mastocytosis - excessive histamine release from mast cells (bone marrow, skin, other organs).

25
Q

gastric mucosal atrophy due to

A

H pylori.

26
Q

5 types o fpancreatic endocrie tumors

A
  1. gastrin (ZES)
  2. insulin (hypoglycemia)
  3. glucagon (hyperglycemia, rahs)
  4. Somatostatin (diarrhea, cholelithihiasis, hyperglycemia)
  5. Vasoactive Intestinal Polypeptide (watery diarreha, hypoK, achlorhydria).
27
Q

Small Intestine Bacterial Overgrowth results in what to levels of: B12, folic acid, iron, Zinc, vitamin A, D, E, K

A

Malabsoprtion leads to decreased all except for increased Folate and vitamin K (dt bacterial synthesis of both).

28
Q

How does a GU bleed precipitate hepatic encephalopathy?

What happens to GABA, glycine, and cat levels?

Tx?

A

GI bleed causes increased nitrogen delivery to gut to form Hb, then converted into ammonia and basorbed into bloodstream. Ammonia enters liver. If liver failures, then buildup of ammonia –> increased GABA (inhibitory) and decreased glutamate/cats (excitatory).

Tx - lactulose to lower blood ammonia levels.

29
Q

A man has a longitudinal tear in his GE-junction. What acid-base disturbance does he probably have?

A

metabolic alkalosis from vomiting. he has mallory-weiss.

30
Q

Breast milk contains all vitamins and minerals except for what two?

A

Vitamin D and K.

31
Q

SPINK1 mutation

A

Renders trypsin insenstitive to cleavage inactivation, resulting in hereditary pancreatitis.

Normal function is to impede trypsinogen that prematurely become activated while in the pancreas.

32
Q

Sx: jaundice
Labs: direct hyperBR
Black liver due to imparied excretion of epinephrine metabolites, appearing as dense pigments in lysosomes.
Absence of biliary transport protein, used in hepatocellular excretion of BR glucuronides into bile canaliculu.

A

Dubin-Johnson

33
Q

Asx conjugated hyperBR. Jaundice. resutls from numerous defects in heptatic uptake and BR pigmetns.

A

Rotor

34
Q

lack of UGT enzyme, so cannot conjugate BR. Kernicterus, death, hyperBR in infants

A

Crigler-Najjar

35
Q

Senescent ceruloplasmin or unabsorbed copper is ecreted into bile and excreted in stool.

**Primary mechanism for copper secretion

A

CUT AND PASTE

36
Q

If a person as a total gastrectomy, what must they have life-long administration of?

A

Water-soluble vitamins

37
Q

Joint pain, LAD, uritcarial rash, HM, RUQ pain. Elevated AST ALT. Mutliple sexual partners.

A

HEp B

38
Q

watery diarreha, hypoK, achlohydria - what is this?

A

Pacnreatic cholera due to high levels of VIP.

39
Q

a two month old presents with jaundice, dark urine, acholic stools. Biopsy reveals intrahepatic bile duct proliferation, protal tract edema, and fibrosis.

A

Biliary atresia obstructs teh extrahepatic bile ducts, causing conjugated hyperBR.

40
Q

Night lindess and corenal ulceration, keratinization (course/dry) skin. What vitamin is deficient and what etiology?

A

Vitamin A. Possibly due to Primary Biliary Cirrhosis - lack of fat soluble vitamin absorption.

41
Q

Presents in elderly patients with dysphagia, halitosis, regurgitation, and recurent aspiration. What is this and what’s the likely etiology?

A

Zenker Diverticulum - diminsihed relaxation of cricopharyngeal muscles during swallowing, resulting in increased intraluminal pressure in oropharynx. May cause mucosa to herniate thorugh zone of mm weakness into posterior hypopharynx.

42
Q

New onset odontophagia in setting of chronic GERD indicates what?

A

ERosive esophagitis and ulcer formation. Dx with upper endoscopy.

43
Q

Sudan III stain tests stool for what?

A

Fat malabsorptin

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